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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) srt2:(2010-2014);srt2:(2011)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) > (2010-2014) > (2011)

  • Resultat 41-50 av 530
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41.
  • Piper, Barbara F, et al. (författare)
  • Cancer-related fatigue
  • 2011
  • Ingår i: The MASCC textbook of cancer supportive care and survivorship. - New York : Springer. - 9781441912244 ; , s. 23-32
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • This chapter describes what is currently known about cancer-related fatigue (CRF) in cancer survivors. Significance and prevalence rates are reviewed and definitions are discussed within the context of the need to develop case definitions and phenotypes to advance the science and practice of CRF. Two conceptual frameworks/models for CRF are identified based on emerging evidence that unify the seemingly disparate underlying mechanisms proposed in the literature. While further testing of these models and their propositions are needed, these models can be used to guide future studies investigating CRF and its underlying relationships with other symptoms such as pain, depression, and insomnia. The National Comprehensive Cancer Network (NCCN) guidelines for the assessment and management of CRF are reviewed. Particular emphasis is given to the assessment and management of the common contributing and treatable factors associated with CRF (i.e., anemia, comorbidities, deconditioning, emotional distress, nutrition, pain, sleep disturbance/insomnia, symptom clusters, and cognitive impairment). Barriers to guideline adherence and exercise prescription are discussed, and patient and provider education is emphasized.
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42.
  • Edlinger, M., et al. (författare)
  • Metabolic syndrome and risk of brain tumour in a large population-based cohort study
  • 2011
  • Ingår i: IEA World Congress of Epidemiology, 7–11 August 2011, Edinburgh International Conference Centre, Edinburgh, Scotland. - : BMJ.
  • Konferensbidrag (refereegranskat)abstract
    • Background: There are few established determinants of brain tumour. We assessed among adults the risk of brain tumour in relation to metabolic syndrome factors. Methods: 580 000 subjects from Sweden, Austria, and Norway were followed for a median of 10 years (Me-Can). Brain tumour information was obtained from national cancer registries. The factors of metabolic syndrome, body mass index, blood pressure, and blood levels of glucose, cholesterol, and triglycerides, were analysed in quintiles and for transformed z-scores (mean of 0 and SD of 1). Cox proportional hazards regression models were applied, stratified by cohort and corrected for measurement error. Results: In total 1312 primary brain tumours were diagnosed during follow-up, predominantly high-grade glioma (n=436) and meningioma (n=348). For meningioma, the HR was increased for systolic blood pressure (HR=1.27 per unit SD, 95% CI 1.03 to 1.57), for diastolic blood pressure (HR=1.29, 95% CI 1.04 to 1.58), and for the combined metabolic syndrome score (HR=1.31, 95% CI 1.11 to 1.54). For high-grade glioma the risk was increased for diastolic blood pressure (HR=1.23, 95% CI 1.01 to 1.50) and triglycerides (HR=1.35, 95% CI 1.05 to 1.72). For both meningioma and high-grade glioma, the risk was more than doubled in the fifth quintiles of diastolic blood pressure compared to the first quintile. For systolic blood pressure the meningioma risk was even larger. Conclusion: Increased blood pressure was related to risk of brain tumour, particularly of meningiomas.
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43.
  • Larsson, Dhana E (författare)
  • Analyses of Dose-Response and Mechanistic Action of Different Anti-Cancer Drugs for Neuroendocrine Tumor Cell Lines
  • 2011
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Cancer is a disease with poor response rates on available treatments. Problems with resistance and intolerance against cancer drugs are major reasons for failure of the drugs. The need to discover new cancer drugs is important. In this thesis screening of new cancer drugs and evaluation of their mechanism of action are discussed. The aim of the thesis was to find new compounds active against neuroendocrine tumors (NETs). In paper I, we screened 1280 substances on two bronchial carcinoid cell lines and one pancreatic carcinoid cell line. Eleven of these compounds were found to have antitumor activity at low concentrations. The most active agents were brefeldin A, emetine, bortezomib and idarubicin, having IC50 values (the concentration of the drug where > 50% of the cells die) < 1μM. In addition, sanguinarine, Bay11-7085, mitoxantrone, doxorubicin, β-lapachone, NSC 95397 and CGP- 74514A were active with IC50 values < 10 μM.  In paper II, additional studies have been undertaken to investigate the combination effect of the most active drugs with conventional cytotoxic drugs used in clinical practice. If synergistic or additive effects are found, drugs with different mechanism of action and toxicity profiles may be combined, making it possible to reduce the toxic effects yet maintaining the antitumor activity. In paper III, studies were undertaken to find the mechanistic action, apoptosis or necrosis, of the drugs NSC 95397, brefeldin A, bortezomib and sanguinarine in NETs. All four drugs were shown to induce caspase-3 activity and nuclear fragmentation/condensation in the neuroendocrine tumor cell lines, indicating that their antitumor activity was induction of apoptosis. In paper IV, the mechanism of action was studied for CGP-74514A and emetine. Both drugs worked by induction of apoptosis. In addition, their cytotoxic activity was studied in a three-dimensional model, the in vitro hollow fiber model. The Hollow Fiber model permits more realistic simulation of in vivo drug effects in a controlled system providing data that more accurately reflects biological responses. Our results showed that the hollow fiber model may be suitable for studies of new drugs in the neuroendocrine tumor cell lines.
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44.
  • Chen, Tianhui, et al. (författare)
  • Circulating sex steroids during pregnancy and maternal risk of non-epithelial ovarian cancer
  • 2011
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 20:2, s. 324-336
  • Tidskriftsartikel (refereegranskat)abstract
    • This is the first prospective study providing initial evidence that elevated androgens play a role in the pathogenesis of SCST. Impact: Our study may note a particular need for larger confirmatory investigations on sex steroids and NEOC. Cancer Epidemiol Biomarkers Prev; 20(2); 324-36. ©2010 AACR.
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45.
  • Carlsson, Jessica, 1984-, et al. (författare)
  • A miRNA expression signature that separates between normal and malignant prostate tissues
  • 2011
  • Ingår i: Cancer Cell International. - : BioMed Central (BMC). - 1475-2867. ; :11, s. 14-
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundMicroRNAs (miRNAs) constitute a class of small non-coding RNAs that post-transcriptionally regulate genes involved in several key biological processes and thus are involved in various diseases, including cancer. In this study we aimed to identify a miRNA expression signature that could be used to separate between normal and malignant prostate tissues.ResultsNine miRNAs were found to be differentially expressed (p <0.00001). With the exception of two samples, this expression signature could be used to separate between the normal and malignant tissues. A cross-validation procedure confirmed the generality of this expression signature. We also identified 16 miRNAs that possibly could be used as a complement to current methods for grading of prostate tumor tissues.ConclusionsWe found an expression signature based on nine differentially expressed miRNAs that with high accuracy (85%) could classify the normal and malignant prostate tissues in patients from the Swedish Watchful Waiting cohort. The results show that there are significant differences in miRNA expression between normal and malignant prostate tissue, indicating that these small RNA molecules might be important in the biogenesis of prostate cancer and potentially useful for clinical diagnosis of the disease.
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46.
  • Hofmann, Jonathan N., et al. (författare)
  • Risk of kidney cancer and chronic kidney disease in relation to hepatitis C virus infection : a nationwide register-based cohort study in Sweden
  • 2011
  • Ingår i: European Journal of Cancer Prevention. - 0959-8278 .- 1473-5709. ; 20:4, s. 326-30
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic hepatitis C virus (HCV) infection is an established cause of liver cancer, and recent studies have suggested a link with kidney cancer. The aim of this study was to evaluate risk of kidney cancer in relation to HCV infection in a nationwide registry-based study of Swedish residents diagnosed with HCV between 1990 and 2006. A total of 43 000 individuals with chronic HCV infection were included, and the mean follow-up time was 9.3 years. Observed kidney cancer incidence and mortality in the cohort were compared with expected values based on the age-adjusted and sex-adjusted rates in the general population. Risk of hospitalization for other chronic kidney disease was also evaluated using Cox proportional hazards regression. No association between HCV infection and risk of kidney cancer was observed [standardized incidence ratio with 1-year lag=1.2; 95% confidence interval (CI): 0.8-1.7]. Risk of hospitalization for noncancer kidney disease was significantly elevated in the HCV cohort, with significantly stronger associations observed among women than among men [hazard ratio=5.8 (95% CI: 4.2-7.9) and 3.9 (95% CI: 3.2-4.8) for women and men, respectively]. Results of this study do not support the hypothesis that chronic HCV infection confers an increased risk of kidney cancer. However, we did find an association between HCV infection and chronic kidney disease, particularly among women. Given inconsistent findings in the literature, it is premature to consider HCV infection to be a risk factor for kidney cancer.
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47.
  • Landgren, Annelie M., et al. (författare)
  • Autoimmune Disease and Subsequent Risk of Developing Alimentary Tract Cancers Among 4.5 Million US Male Veterans
  • 2011
  • Ingår i: Cancer. - : Wiley. - 0008-543X .- 1097-0142. ; 117:6, s. 1163-1171
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Autoimmunity is clearly linked with hematologic malignancies, but less is known about autoimmunity and alimentary tract cancer risk, despite the specific targeting of alimentary organs and tissues by several autoimmune diseases. The authors therefore conducted the first systematic evaluation of a broad range of specific autoimmune diseases and risk for subsequent alimentary tract cancer. METHODS: On the basis of 4,501,578 US male veterans, the authors identified 96,277 men who developed alimentary tract cancer during up to 26.2 years of follow-up. By using Poisson regression methods, the authors calculated relative risks (RRs) and 95% confidence intervals. RESULTS: A history of autoimmune disease with localized alimentary tract effects generally increased cancer risks in the organ(s) affected by the autoimmune disease, such as primary biliary cirrhosis and liver cancer (RR, 6.01; 95% confidence interval [Cl], 4.76-7.57); pernicious anemia and stomach cancer (RR, 3.17; 95% Cl, 2.47-4.07); and ulcerative colitis and small intestine, colon, and rectal cancers (RR, 2.53; 95% Cl, 1.05-6.11; RR, 2.06; 95% Cl, 1.70-2.48; and RR, 2.07; 95% Cl, 1.62-2.64, respectively). In addition, a history of celiac disease, reactive arthritis (Reiter disease), and systemic sclerosis all were associated significantly with increased risk of esophageal cancer (RR, 1.86-2.86). Autoimmune diseases without localized alimentary tract effects generally were not associated with alimentary tract cancer risk, with the exception of decreased risk for multiple alimentary tract cancers associated with a history of multiple sclerosis. CONCLUSIONS: These findings support the importance of localized inflammation in alimentary tract carcinogenesis. Future research is needed to confirm the findings and improve understanding of underlying mechanisms by which autoimmune diseases contribute to alimentary tract carcinogenesis. Cancer 2011;117:1163-71. Published 2010 by the American Cancer Society*
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48.
  • Löf-Öhlin, Zarah M., et al. (författare)
  • Promoter methylation in the PTCH gene in cervical epithelial cancer and ovarian cancer tissue as studied by eight novel Pyrosequencing (R) assays
  • 2011
  • Ingår i: International Journal of Oncology. - : Spandidos Publications. - 1019-6439 .- 1791-2423. ; 38:3, s. 685-692
  • Tidskriftsartikel (refereegranskat)abstract
    • DNA methylation status in the CpG sites of promoter regions in cancer-related genes, such as PTCH, has traditionally been investigated using either dye-terminator sequencing or methylation-specific PCR. We aimed to study the PTCH gene promoter methylation in gynecological cancers with a method that gives a quantitative measure of the methylation status of the promoter region of the studied gene, and for this purpose, we designed novel Pyrosequencing-based assays. Bisulfite-treated genomic DNA (bsDNA) was amplified by standard PCR and applied to novel Pyrosequencing(R) assays, in order to measure the methylated fraction (%) at each CpG site of the PTCH gene promoter. We analyzed 22 squamous cell cervical cancer tissue specimens (11 with good and 11 with poor outcomes after radiotherapy) and 5 ovarian cancer tissue specimens matched with 5 normal ovarian tissue specimens. Six optimized PCR protocols which generated 8 Pyrosequencing assays covering 63 CpG sites in the promoter regions 1 and 2 as well as the previously unanalyzed promoter region 3 in the PTCH gene were developed. The 27 tumor tissue specimens and 5 normal tissues did not show any methylation within any of the 63 CpG sites. Our data suggest that methylation of the PTCH promoter is not a high-prevalence feature of squamous cell cervical cancer or ovarian cancer, but Pyrosequencing assays are a good method for studying promoter methylation.
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49.
  • Lööf, Jasmine, 1982-, et al. (författare)
  • Impact of PINCH expression on survival in colorectal cancer patients
  • 2011
  • Ingår i: BMC CANCER. - : BioMed Central. - 1471-2407. ; 11:103
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The adaptor protein PINCH is overexpressed in the stroma of several types of cancer, and is an independent prognostic marker in colorectal cancer. In this study we further investigate the relationship of PINCH and survival regarding the response to chemotherapy in colorectal cancer. Results: Paraffin-embedded tissue sections from 251 primary adenocarcinomas, 149 samples of adjacent normal mucosa, 57 samples of distant normal mucosa and 75 lymph node metastases were used for immunohistochemical staining. Stromal staining for PINCH increased from normal mucosa to primary tumour to metastasis. Strong staining in adjacent normal mucosa was related to worse survival independently of sex, age, tumour location, differentiation and stage (p = 0.044, HR, 1.60, 95% Cl, 1.01-2.52). PINCH staining at the invasive margin tended to be related to survival (p = 0.051). In poorly differentiated tumours PINCH staining at the invasive margin was related to survival independently of sex, age and stage (p = 0.013, HR, 1.90, 95% Cl, 1.14-3.16), while in better differentiated tumours it was not. In patients with weak staining, adjuvant chemotherapy was related to survival (p = 0.010, 0.013 and 0.013 in entire tumour area, invasive margin and inner tumour area, respectively), but not in patients with strong staining. However, in the multivariate analysis no such relationship was seen. Conclusions: PINCH staining in normal adjacent mucosa was related to survival. Further, PINCH staining at the tumour invasive margin was related to survival in poorly differentiated tumours but not in better differentiated tumours, indicating that the impact of PINCH on prognosis was dependent on differentiation status.
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50.
  • Margolin, Sara, et al. (författare)
  • A randomised feasibility/phase II study (SBG 2004-1) with dose-dense/tailored epirubicin, cyclophoshamide (EC) followed by docetaxel (T) or fixed dosed dose-dense EC/T versus T, doxorubicin and C (TAC) in node-positive breast cancer.
  • 2011
  • Ingår i: Acta Oncologica. - : Informa Healthcare. - 0284-186X .- 1651-226X. ; 50:1, s. 35-41
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of the study was to evaluate the feasibility of tailored and dose-dense epirubicin and cyclophosphamide followed by docetaxel as adjuvant breast cancer therapy. Material and methods. Patients with node-positive breast cancer received either four cycles of biweekly and tailored EC (epirubicin 38-60-75-90-105-120 mg/m(2), cyclophosphamide 450-600-900-1200 mg/m(2)) followed by four cycles of docetaxel (60-75-85-100 mg/m(2)) (arm A) or the same regimen with fixed doses (E(90)C(600) + 4 → T(75) + 4) (arm B) or docetaxel, doxorubicin and cyclophosphamide (T(75)A(50)C(500)) every three weeks for six cycles (arm C). All patients received G-CSF support and prophylactic ciprofloxacin. Results. One-hundred and twenty-four patients were randomised in the study. In the A, B and C arm, 17% 19% and 3% of the patients had one or more cycles delayed due to side-effects whereas 24%, 5% and 15% experienced a grade 3 infection or febrile neutropenia. After the introduction of an extra week between the EC and T parts in the A and B arms, grade 3 hand-foot-skin reactions were reduced from 5 to 0.2%. Twenty-nine percent (A and B) and 20% (C) of the patients were hospitalised due to side-effects. Discussion. Dose-dense and tailored EC/T can be given with manageable toxicity and is after adjustment presently studied in the phase III Panther trial.
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